Mohamed Ibrahim, DinaTarek, GinaHani Makram, MerihaneKamal Yassin, Yasmin2024-06-042024-06-042023Faculty Of Pharmacy Graduation Projecthttp://repository.msa.edu.eg/xmlui/handle/123456789/6010Faculty Of Pharmacy Graduation ProjectMyocardial infarction is the main leading cause of mortality world widely. In 2015, it is predicted that 7.4 million people died as a result of coronary heart disease. CVDs are predicted to kill 23.6 million individuals by 2030. Decreased or complete obstruction of the blood flow to part of the myocardium is the main cause of myocardial infarction. For the vast majority of those suffering from non-ST-segment elevation myocardial infarction (NSTEMI) as opposed to STsegment elevation myocardial infarction, it accounts for more than 15% of mortality each year. Myocardial infarction encompasses four different mechanisms which are: atherosclerosis development, deterioration of the formed fibrous plaque, thrombus formation and myocardial cell death. Tofacitinib is the drug under investigation in this study as it is suggested to have a cytoprotective effect against MI since it acts as inhibitor of the JAKs family which interferes with JAK/STAT signaling that occur following the inflammation that occur during myocardial infarction. This study aims to investigate both the relation between kinase inhibitors and myocardial infarction and the possible cytoprotective effect of Tofacitinib on experimentallyinduced myocardial infarction. In this recent study, 18 albino mice were used and randomly allocated into three groups. Group (A) was injected with saline only, Group (B) was injected with Isoprenaline HCl (100mg/kg) subcutaneously for induction of myocardial infarction and Group (C) was treated with Tofacitinib after receiving isoprenaline for 14 days. The parameters that were assessed were TNF-ὰ, cardiac troponin I, creatine kinase –MB, STAT-3, Lnc-Xist, NF-κB, mTor, IL-6 and there was histopathological examination. The results that were obtained from laboratory investigation of the previous parameters and histopathological examination proved the cytoprotective effect of Tofacitinib against MI as well as its ability to inhibit the inflammation and necrosis of the cardiomyctes that occur following the occurrence of MI. Therefore, Tofacitinib could be a used as a promising treatment and prophylaxis from myocardial infarctionenMSAOctober University for Modern Science and ArtsUniversity for Modern Science and Artsجامعة أكتوبر للعلوم الحديثة والآدابPHARMACOLOGYOther